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Updated: Jun 12, 2026

Isolation of Whole Cell Protein Lysates from Mouse Facial Processes and Cultured Palatal Mesenchyme Cells for Phosphoprotein Analysis
Published on: April 1, 2022
Sulfotransferase Ndst1 is needed for mandibular and TMJ development
T Yasuda1, C Mundy, T Kinumatsu
1Department of Orthopaedic Surgery, Thomas Jefferson University College of Medicine, 1015 Walnut Street, Curtis Building Room 501, Philadelphia, PA 19107, USA.
Heparan sulfate proteoglycans (HS-PGs) are crucial for jaw and temporomandibular joint (TMJ) development. Disrupting their sulfation via Ndst1 deficiency leads to severe defects, including TMJ absence and facial asymmetry.
Area of Science:
- Developmental Biology
- Molecular Biology
- Biochemistry
Background:
- Heparan sulfate proteoglycans (HS-PGs) are key regulators of cellular processes.
- Their specific roles in mandibular and temporomandibular joint (TMJ) development remain largely unknown.
- Ndst1 catalyzes the critical sulfation of HS-PG glycosaminoglycan chains.
Purpose of the Study:
- To investigate the function of Ndst1-dependent HS sulfation in mandibular and TMJ development.
- To elucidate the molecular mechanisms underlying HS-PG involvement in craniofacial morphogenesis.
Main Methods:
- Generation and analysis of mice lacking Golgi-associated N-sulfotransferase 1 (Ndst1).
- Phenotypic assessment of Ndst1-null embryos, including morphological, histological, and molecular analyses.
- Evaluation of tooth germ development, angiogenesis, apoptosis, and Indian hedgehog (Ihh) signaling.
Main Results:
- Ndst1-null embryos displayed variable phenotypic severity, with some lacking TMJ and condyle.
- Severely affected mutants showed abnormal tooth germs, poor angiogenesis, and increased apoptosis.
- Mildly affected mutants exhibited condylar growth plate dysfunction, altered Ihh signaling, ectopic ossification, and facial asymmetry.
Conclusions:
- Ndst1-dependent HS sulfation is essential for proper mandibular and TMJ formation.
- HS-PGs regulate craniofacial development by modulating Ihh signaling topography and activity.
- Defects in HS sulfation may contribute to conditions like hemifacial microsomia.
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